ArticleMedical microbiology and immunology2004
Nitric oxide donors inhibit the coxsackievirus B3 proteinases 2A and 3C in vitro, virus production in cells, and signs of myocarditis in virus-infected mice.
Article in Medical microbiology and immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 55 citations in OpenAlex.
- Article
- Protein-S-nitrosylation of human cytomegalovirus pp65 reduces its ability to undermine cGAS.Journal of virology · 2025Article
- Protein S-Nitrosylation: A Chemical Modification with Ubiquitous Biological Activities.The protein journal · 2024Review
- Viral proteases activate the CARD8 inflammasome in the human cardiovascular system.The Journal of experimental medicine · 2022Article
- The potential role of inhaled nitric oxide for postexposure chemoprophylaxis of COVID-19.Journal, genetic engineering & biotechnology · 2021Article
- Interferon-stimulated gene products as regulators of central carbon metabolism.The FEBS journal · 2021Article
- Nitric oxide and viral infection: Recent developments in antiviral therapies and platforms.Applied materials today · 2021Review
- Inhibition of endogenous hydrogen sulfide production improves viral elimination in CVB3-infected myocardium in mice.Pediatric research · 2019Article
- Activation of toll-like receptor signaling pathways leading to nitric oxide-mediated antiviral responses.Archives of virology · 2016Review
- Article
- Nitric oxide synthases, S-nitrosylation and cardiovascular health: from molecular mechanisms to therapeutic opportunities (review).Molecular medicine reports · 2015Review
- The role of myeloid cell activation and arginine metabolism in the pathogenesis of virus-induced diseases.Frontiers in immunology · 2014Review
- Gaseous nitric oxide reduces influenza infectivity in vitro.Nitric oxide : biology and chemistry · 2013Article
- Pharmacological and biological antiviral therapeutics for cardiac coxsackievirus infections.Molecules (Basel, Switzerland) · 2011Review
- Mesenchymal stem cells improve murine acute coxsackievirus B3-induced myocarditis.European heart journal · 2011Article
- Nitric oxide and redox mechanisms in the immune response.Journal of leukocyte biology · 2011Review
- Mesenchymal stem cells and inflammatory cardiomyopathy: cardiac homing and beyond.Cardiology research and practice · 2011Article
- The human rhinovirus: human-pathological impact, mechanisms of antirhinoviral agents, and strategies for their discovery.Medicinal research reviews · 2011Review
- Human cardiac-derived adherent proliferating cells reduce murine acute Coxsackievirus B3-induced myocarditis.PloS one · 2011Article
- Role of epithelial nitric oxide in airway viral infection.Free radical biology & medicine · 2006Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The antiviral effect of nitric oxide (NO)-releasing compounds was investigated. Using bacterially expressed and purified proteinases 2A and 3C of coxsackievirus B3, in vitro assays demonstrated the inhibition of the 2A proteinase activity in the presence of S-nitroso- N-acetyl-penicillamine (SNAP), 3-morpholinosydnonimine (SIN-1), 4-phenyl-3-furoxancarbonitrile (PFC), glyceryl trinitrate (GTN), and isosorbide dinitrate (ISDN). Sodium nitroprusside (SNP), which releases NO after metabolization, had no effect. The 3C proteinase was inactivated by SNAP, GTN, and ISDN. The vasodilators GTN and ISDN, widely used in the treatment of angina pectoris, exhibited antiviral activity in CVB3-infected GMK cells. CVB3-infected NMRI outbred mice showed significantly reduced signs of myocarditis after treatment with GTN or ISDN. Inhibitors of the cellular inducible NO synthase (iNOS) such as N(G)-nitro-L-arginine methyl ester (L-NAME), N(G)-nitro-L-arginine (L-NNA), and S-methyl-isothiourea (SMT), had no deleterious effect on CVB3-infected NMRI mice, indicating that endogenous NO synthesis is unlikely to be a major defense mechanism after enterovirus infection of outbred mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.